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Ella Livni - One of the best experts on this subject based on the ideXlab platform.
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in vitro release of interferon gamma and Macrophage Migration Inhibition factor in drug induced urticaria and angioedema
Acta Dermato-venereologica, 1999Co-Authors: Ella Livni, Moshe Lapidoth, Sima HalevyAbstract:: T-cells are involved in the pathogenesis of cutaneous drug reactions. T-cell phenotype and cytokine release pattern in rivo and in vitro might correlate with the type of immune response involved in cutaneous drug reactions. In vitro release of interferon-gamma and Macrophage Migration Inhibition factor (MIF) from peripheral blood lymphocytes, following in vitro challenge with the suspected unmodified drugs, was studied in 12 patients with drug-induced urticaria and/or angioedema and in two group-matched controls. The occurrence of positive interferon-gamma and MIF responses was significantly higher in patients with drug-induced urticaria and/or angioedema than in controls. The sensitivity and specificity of the interferon-gamma test (50% and 92%, respectively) were similar to that of the MIF test (58% and 96%, respectively). Percentage agreement between both tests was 80.9 (kappa = 0.76). In vitro release of interferon-gamma and MIF in drug-induced urticaria and/or angioedema suggests a drug-specific immune response, and may implicate the drug as a possible inducer of the reaction.
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The role of Macrophage Migration Inhibition factor in toxic epidermal necrolysis.
International Journal of Dermatology, 1997Co-Authors: Sima Halevy, Ella LivniAbstract:Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A Macrophage Migration Inhibition factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The Macrophage Migration Inhibition factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P
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the role of Macrophage Migration Inhibition factor in toxic epidermal necrolysis
International Journal of Dermatology, 1997Co-Authors: Sima Halevy, Ella LivniAbstract:Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A Macrophage Migration Inhibition factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The Macrophage Migration Inhibition factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P<0.05) than that recorded in the controls (0/17). The MIF test results in TEN patients and controls are summarized in Table 1.
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Macrophage Migration Inhibition factor release in lichenoid drug eruptions
Journal of The American Academy of Dermatology, 1993Co-Authors: Sima Halevy, Miriam Sandbank, Ella LivniAbstract:Lichenoid drug eruption (DE) that can clinically and histologically resemble lichen planus (LP) can be induced by gold, thiazide diuretics, quinidine, and other agents. 1, 2 Lichenoid DE, which in general spares the mucous membranes, may be photodistributed or nonphotodistributed.P Common causes of photodistributed lichenoid DE are thiazide diuretics-" and quinidine.': 5 The mechanism by which drugs induce a lichenoid tissue reaction is unknown. Recent observations support a critical role of helper/inducer T lymphocytes in lichenoid tissue reaction." In isolated cases of lichenoid photosensitive DE induced by hydrochlorothiazide or quinidine, positive Macrophage Migration Inhibition factor (MIF) responses toward the offending drugs were recorded.f5 MIF is a lymphokine released from sensitized T lymphocytes by an appropriate antigen. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in animal models and in humans.71O Furthermore, MIF release has been recently reported to be valuable in the diagnosis of adverse drug reactions, including DE,ll-15 The present study was conducted to evaluate MIF release in patients with lichenoid DE induced by various drugs.
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Macrophage Migration Inhibition factor as a diagnostic aid in drug eruptions
Harefuah, 1991Co-Authors: Halevy S, Marcelo H Grunwald, Miriam Sandbank, Buimovice B, Ella LivniAbstract:: The diagnostic value of the Macrophage Migration Inhibition factor (MIF) test was evaluated in 90 patients with the clinical diagnosis of drug eruption. There were 40 males and 50 females who ranged in age from 15-84 years (mean 61.0). Controls were 120 patients being treated with drugs without adverse reactions and 21 patients with dermatologic disorders unrelated to drugs. Positive MIF responses for 1 or more drugs were observed in 71.1% of the patients with drug eruptions as compared to 4.2% and 9.5% of the control groups, respectively (p less than 0.001 for both). The proportion of positive MIF responses in those in whom drugs were implicated (45.2%) was significantly greater (p less than 0.0001) than in those with eruptions in whom drugs were not implicated (18%). The MIF test may be of aid in the diagnosis of drug eruptions and in the identification of the offending drugs.
Sima Halevy - One of the best experts on this subject based on the ideXlab platform.
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in vitro release of interferon gamma and Macrophage Migration Inhibition factor in drug induced urticaria and angioedema
Acta Dermato-venereologica, 1999Co-Authors: Ella Livni, Moshe Lapidoth, Sima HalevyAbstract:: T-cells are involved in the pathogenesis of cutaneous drug reactions. T-cell phenotype and cytokine release pattern in rivo and in vitro might correlate with the type of immune response involved in cutaneous drug reactions. In vitro release of interferon-gamma and Macrophage Migration Inhibition factor (MIF) from peripheral blood lymphocytes, following in vitro challenge with the suspected unmodified drugs, was studied in 12 patients with drug-induced urticaria and/or angioedema and in two group-matched controls. The occurrence of positive interferon-gamma and MIF responses was significantly higher in patients with drug-induced urticaria and/or angioedema than in controls. The sensitivity and specificity of the interferon-gamma test (50% and 92%, respectively) were similar to that of the MIF test (58% and 96%, respectively). Percentage agreement between both tests was 80.9 (kappa = 0.76). In vitro release of interferon-gamma and MIF in drug-induced urticaria and/or angioedema suggests a drug-specific immune response, and may implicate the drug as a possible inducer of the reaction.
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The role of Macrophage Migration Inhibition factor in toxic epidermal necrolysis.
International Journal of Dermatology, 1997Co-Authors: Sima Halevy, Ella LivniAbstract:Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A Macrophage Migration Inhibition factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The Macrophage Migration Inhibition factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P
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the role of Macrophage Migration Inhibition factor in toxic epidermal necrolysis
International Journal of Dermatology, 1997Co-Authors: Sima Halevy, Ella LivniAbstract:Patient A A 60-year-old man developed toxic epidermal necrolysis (TEN) following several weeks of treatment with two kinds of drug: co-trimoxazole and acetazolamide. On the basis of time relationship data, both drugs could be considered as the inducers of the cutaneous reaction.1 Guide fables indicated that co-trimoxazole is one of the most common inducers of TEN, whereas acetazolamide has been reported as a possible uncommon inducer of TEN.1–3 Drug intake was stopped, and treatment with prednisone (120 mg/day) was instituted, followed by a gradual tapering of the dosage. A month later, complete remission of the skin lesions was observed. A Macrophage Migration Inhibition factor (MIF) test was performed towards the drugs taken, in an attempt to identify the offending drug. The Macrophage Migration Inhibition factor (MIF) test was positive towards co-trimoxazole and negative for acetazolamide. Positive MIF responses towards co-trimoxazole were not recorded in ten control patients (control I) treated with the drug with no manifestations of drug eruption. Patient B TEN was diagnosed in an 84-year-old man treated prior to the appearance of the eruption with two kinds of drug: furosemide, which had been taken for several weeks, and nitrofurantoin, which had been taken for 3 months. On the basis of time relationship data, furosemide was suspected to be the offending drug; however, guide tables indicated nitrofurantoin as a possible inducer of TEN,3 whereas the role of furosemide (a sulfa drug) as an inducer of TEN has not yet been reported. Drug intake was stopped, and following supportive treatment, without the addition of corticosteroids, the skin lesions disappeared 3 weeks later. A MIF test was performed towards furosemide and nitrofurantoin. The MIF test was positive towards furosemide and negative for nitrofurantoin. Positive MIF responses towards furosemide were not recorded in seven control patients (control II) treated with the drug with no manifestations of drug eruption. The MIF test technique The MIF test was performed according to the modified method of Livni et al.4 A Migration index of 0.80 or less at one or more of the drug concentrations was considered to be a positive MIF test. Statistical analysis Statistical analysis of MIF test results in TEN patients and controls was performed using Fisher's exact test (F.E.T.). The occurrence of positive MIF responses towards drugs recorded in TEN patients (2/4) was significantly higher (P<0.05) than that recorded in the controls (0/17). The MIF test results in TEN patients and controls are summarized in Table 1.
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allergic vasculitis induced by decapeptyl confirmation by Macrophage Migration Inhibition factor mif test
European Journal of Obstetrics & Gynecology and Reproductive Biology, 1993Co-Authors: Boaz Amichai, Marcelo H Grunwald, Sima HalevyAbstract:Abstract A case of allergic vasculitis of the skin following treatment with Decapeptyl ® ( d -Trp 6 -LHRH) for in vitro fertilization is described. The possible role of an allergic mechanism in this reaction has been suggested by a positive Macrophage Migration Inhibition factor (MIF) test toward the drug.
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Macrophage Migration Inhibition factor release in lichenoid drug eruptions
Journal of The American Academy of Dermatology, 1993Co-Authors: Sima Halevy, Miriam Sandbank, Ella LivniAbstract:Lichenoid drug eruption (DE) that can clinically and histologically resemble lichen planus (LP) can be induced by gold, thiazide diuretics, quinidine, and other agents. 1, 2 Lichenoid DE, which in general spares the mucous membranes, may be photodistributed or nonphotodistributed.P Common causes of photodistributed lichenoid DE are thiazide diuretics-" and quinidine.': 5 The mechanism by which drugs induce a lichenoid tissue reaction is unknown. Recent observations support a critical role of helper/inducer T lymphocytes in lichenoid tissue reaction." In isolated cases of lichenoid photosensitive DE induced by hydrochlorothiazide or quinidine, positive Macrophage Migration Inhibition factor (MIF) responses toward the offending drugs were recorded.f5 MIF is a lymphokine released from sensitized T lymphocytes by an appropriate antigen. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in animal models and in humans.71O Furthermore, MIF release has been recently reported to be valuable in the diagnosis of adverse drug reactions, including DE,ll-15 The present study was conducted to evaluate MIF release in patients with lichenoid DE induced by various drugs.
Miriam Sandbank - One of the best experts on this subject based on the ideXlab platform.
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Macrophage Migration Inhibition factor release in lichenoid drug eruptions
Journal of The American Academy of Dermatology, 1993Co-Authors: Sima Halevy, Miriam Sandbank, Ella LivniAbstract:Lichenoid drug eruption (DE) that can clinically and histologically resemble lichen planus (LP) can be induced by gold, thiazide diuretics, quinidine, and other agents. 1, 2 Lichenoid DE, which in general spares the mucous membranes, may be photodistributed or nonphotodistributed.P Common causes of photodistributed lichenoid DE are thiazide diuretics-" and quinidine.': 5 The mechanism by which drugs induce a lichenoid tissue reaction is unknown. Recent observations support a critical role of helper/inducer T lymphocytes in lichenoid tissue reaction." In isolated cases of lichenoid photosensitive DE induced by hydrochlorothiazide or quinidine, positive Macrophage Migration Inhibition factor (MIF) responses toward the offending drugs were recorded.f5 MIF is a lymphokine released from sensitized T lymphocytes by an appropriate antigen. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in animal models and in humans.71O Furthermore, MIF release has been recently reported to be valuable in the diagnosis of adverse drug reactions, including DE,ll-15 The present study was conducted to evaluate MIF release in patients with lichenoid DE induced by various drugs.
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Macrophage Migration Inhibition factor as a diagnostic aid in drug eruptions
Harefuah, 1991Co-Authors: Halevy S, Marcelo H Grunwald, Miriam Sandbank, Buimovice B, Ella LivniAbstract:: The diagnostic value of the Macrophage Migration Inhibition factor (MIF) test was evaluated in 90 patients with the clinical diagnosis of drug eruption. There were 40 males and 50 females who ranged in age from 15-84 years (mean 61.0). Controls were 120 patients being treated with drugs without adverse reactions and 21 patients with dermatologic disorders unrelated to drugs. Positive MIF responses for 1 or more drugs were observed in 71.1% of the patients with drug eruptions as compared to 4.2% and 9.5% of the control groups, respectively (p less than 0.001 for both). The proportion of positive MIF responses in those in whom drugs were implicated (45.2%) was significantly greater (p less than 0.0001) than in those with eruptions in whom drugs were not implicated (18%). The MIF test may be of aid in the diagnosis of drug eruptions and in the identification of the offending drugs.
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Macrophage Migration Inhibition factor mif in drug eruption
Archives of Dermatology, 1990Co-Authors: Sima Halevy, Marcelo H Grunwald, Miriam Sandbank, Bella Buimovice, H Joshua, Ella LivniAbstract:• A controlled study was conducted to evaluate the Macrophage Migration Inhibition factor test as a diagnostic aid in 50 patients with drug eruption. Two groups of patients served as controls: group A, 110 patients being treated with drugs without known cutaneous adverse reactions, and group B, 15 patients suffering from dermatologic disorders unrelated to drugs being taken. Positive Macrophage Migration Inhibition factor responses were found toward a variety of drugs in 35 (70%) of the patients with drug eruptions, with no relation to the type of eruption or the duration of drug intake. The percentage of positive Macrophage Migration Inhibition factor responses toward drugs in the patients with drug eruptions was higher than that in the two control groups (4.5% and 6.7%, respectively). The percentage of positive Macrophage Migration Inhibition factor responses recorded for clinically "suspected" drugs was significantly higher than that recorded for the "nonsuspected" drugs. (Arch Dermatol.1990;126:48-51)
Moshe Lapidoth - One of the best experts on this subject based on the ideXlab platform.
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in vitro release of interferon gamma and Macrophage Migration Inhibition factor in drug induced urticaria and angioedema
Acta Dermato-venereologica, 1999Co-Authors: Ella Livni, Moshe Lapidoth, Sima HalevyAbstract:: T-cells are involved in the pathogenesis of cutaneous drug reactions. T-cell phenotype and cytokine release pattern in rivo and in vitro might correlate with the type of immune response involved in cutaneous drug reactions. In vitro release of interferon-gamma and Macrophage Migration Inhibition factor (MIF) from peripheral blood lymphocytes, following in vitro challenge with the suspected unmodified drugs, was studied in 12 patients with drug-induced urticaria and/or angioedema and in two group-matched controls. The occurrence of positive interferon-gamma and MIF responses was significantly higher in patients with drug-induced urticaria and/or angioedema than in controls. The sensitivity and specificity of the interferon-gamma test (50% and 92%, respectively) were similar to that of the MIF test (58% and 96%, respectively). Percentage agreement between both tests was 80.9 (kappa = 0.76). In vitro release of interferon-gamma and MIF in drug-induced urticaria and/or angioedema suggests a drug-specific immune response, and may implicate the drug as a possible inducer of the reaction.
M A Zhongfu - One of the best experts on this subject based on the ideXlab platform.
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role of Macrophage Migration Inhibition factor and high sensitive c reactive protein in carotid atherosclerosis and acute cerebral infarction
Journal of Tropical Medicine, 2008Co-Authors: M A ZhongfuAbstract:Objective To investigate the relationship between the levels of Macrophage Migration Inhibition factor(MIF) and high-sensitive C-reactive protein (hs-CRP),and the incidence of carotid atherosclerosis and acute cerebral infarction. Method One hundred and three patients with first-ever cerebral infarction and 40 normal control subjects were studied. The levels of serum MIF were determined by double antibody enzyme-linked immunosorbent assay,and the levels of serum hs-CRP were measured by immunonephelometric assay. The thickness of carotid intima-media was assessed by carotid ultrasonography.Neurological deficit scores were determined in patients with acute cerebral infarction. Result The levels of serum MIF and hs-CRP in patients with acute cerebral infarction were significantly higher than the normal control subjects (P 0.01).The levels of serum MIF and hs-CRP in unstable plaque groups (mixed and soft plaque group) were significantly higher than those in stable plaque group (hard plaque group) and rough intima group (P0.01). The levels of serum MIF and hs-CRP were positively correlated with the neurological deficit scores in patients with acute cerebral infartion. Conclusion The levels of serum MIF and hs-CRP in patients with acute cerebral infarction may reflect the features and stability of carotid artery plague. It may be used as an index to indicate the severity of cerebral infarction in clinical practice.
