Total and specific IgE levels in patients with atopic dermatitis. The correlation between prick testing, clinical history of allergy, and in vitro quantification of IgE during clinical exacerbation and remission*

1979 ◽  
Vol 4 (2) ◽  
pp. 187-195 ◽  
Author(s):  
RONA M. MacKIE ◽  
SUSAN J. COBB ◽  
REBECCA E.I. COCHRAN ◽  
J. THOMSONS
Keyword(s):  
Atopic Dermatitis ◽  
Clinical History ◽  
Specific Ige ◽  
History Of

Component resolved diagnostics in peanut sensitized children with and without a history of clinical reaction

2020 ◽  
Vol 41 (5) ◽  
pp. 336-340
Author(s):  
Yasmin Hamzavi Abedi ◽  
Cristina P. Sison ◽  
Punita Ponda
Keyword(s):  
Retrospective Chart Review ◽  
Clinical History ◽  
Specific Ige ◽  
Exact Test ◽  
Ara H 1 ◽  
Sige Level ◽  
History Of ◽  
Laboratory Procedures ◽  
Ige Mediated ◽  
The Relationship

Background: Serum Peanut-specific-IgE (PN-sIgE) and peanut-component-resolved-diagnostics (CRD) are often ordered simultaneously in the evaluation for peanut allergy. Results often guide the plans for peanut oral challenge. However, the clinical utility of CRD at different total PN-sIgE levels is unclear. A commonly used predefined CRD Ara h2 cutoff value in the literature predicting probability of peanut challenge outcomes is 0.35kUA/L. Objective: To examine the utility of CRD in patients with and without a history of clinical reactivity to peanut (PN). Methods: This was a retrospective chart review of 196 children with PN-sIgE and CRD testing, of which, 98 patients had a clinical history of an IgE-mediated reaction when exposed to PN and 98 did not. The Fisher's exact test was used to assess the relationship between CRD and PN-sIgE at different cutoff levels, McNemar test and Gwet’s approach (AC1 statistic) were used to examine agreement between CRD and PN-sIgE, and logistic regression was used to assess differences in the findings between patients with and without reaction history. Results: Ara h 1, 2, 3, or 9 (ARAH) levels ≤0.35 kUA/L were significantly associated with PN-sIgE levels <2 kUA/L rather than ≥2 kUA/L (p < 0.0001). When the ARAH threshold was increased to 1 kUA/L and 2 kUA/L, these thresholds were still significantly associated with PN-sIgE levels of <2, <5, and <14 kUA/L. These findings were not significantly different in patients with and without a history of clinical reactivity. Conclusion: ARAH values correlated with PN-sIgE. Regardless of clinical history, ARAH levels are unlikely to be below 0.35, 1, or 2 kUA/L if the PN-sIgE level is >2 kUA/L. Thus, if possible, practitioners should consider PN-sIgE rather than automatically ordering CRD with PN-sIgE every time. Laboratory procedures that allow automatically and reflexively adding CRD when the PN-sIgE level is ≤5 kUA/L can be helpful. However, further studies are needed in subjects with challenge-proven PN allergy.

Increased thromboxane biosynthesis in patients with polycythemia vera: evidence for aspirin-suppressible platelet activation in vivo [see comments]

Blood ◽  
1992 ◽  
Vol 80 (8) ◽  
pp. 1965-1971 ◽  
Author(s):  
R Landolfi ◽  
G Ciabattoni ◽  
P Patrignani ◽  
MA Castellana ◽  
E Pogliani ◽  
...  
Keyword(s):  
Polycythemia Vera ◽  
Clinical History ◽  
Current Treatment ◽  
Lipoxygenase Pathway ◽  
Binding Characteristics ◽  
History Of ◽  
Thrombotic Complications ◽  
Excretion Rates

Abstract Increased thromboxane (TX) production and modified aspirin sensitivity has been detected in vitro in platelets isolated from patients with polycythemia vera. To verify the relevance of these capacity-related measurements to the actual rate of TXA2 biosynthesis in vivo and its suppression by oral aspirin, we have investigated the urinary excretion of major enzymatic metabolites of TXB2 in 17 patients with polycythemia vera and 23 gender- and age-matched controls. Urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2 were measured by previously validated radioimmunoassays. In addition, urinary immunoreactive leukotriene (LT) E4 was measured to explore the 5-lipoxygenase pathway of arachidonate metabolism. Polycythemic patients had significantly (P < .001) higher excretion rates of both 11-dehydro-TXB2 (1,033 +/- 1,050 v 117 +/- 45 pmol/mmol creatinine; mean +/- SD) and 2,3-dinor-TXB2 (725 +/- 676 v 82 +/- 43 pmol/mmol creatinine) than controls. In contrast, urinary LTE4 was not significantly different. Enhanced metabolite excretion did not correlate with the platelet count or with the hematocrit value, and was not related to the current treatment or to a clinical history of thrombotic complications. Platelet TX receptor studies did not show any significant changes in the binding characteristics of two different ligands. A platelet-selective regimen of aspirin therapy (50 mg/d for 7 to 14 days) was associated with greater than 80% suppression in metabolite excretion in nine patients. These results are consistent with abnormal stimuli operating in polycythemia vera to induce a selective enhancement in the platelet biosynthesis of TXA2 without changes in receptor binding. This in vivo abnormality in platelet biochemistry can be largely suppressed by low doses of aspirin.

scholarly journals Increased thromboxane biosynthesis in patients with polycythemia vera: evidence for aspirin-suppressible platelet activation in vivo [see comments]

Blood ◽  
1992 ◽  
Vol 80 (8) ◽  
pp. 1965-1971 ◽  
Author(s):  
R Landolfi ◽  
G Ciabattoni ◽  
P Patrignani ◽  
MA Castellana ◽  
E Pogliani ◽  
...  
Keyword(s):  
Polycythemia Vera ◽  
Clinical History ◽  
Current Treatment ◽  
Lipoxygenase Pathway ◽  
Binding Characteristics ◽  
History Of ◽  
Thrombotic Complications ◽  
Excretion Rates

Increased thromboxane (TX) production and modified aspirin sensitivity has been detected in vitro in platelets isolated from patients with polycythemia vera. To verify the relevance of these capacity-related measurements to the actual rate of TXA2 biosynthesis in vivo and its suppression by oral aspirin, we have investigated the urinary excretion of major enzymatic metabolites of TXB2 in 17 patients with polycythemia vera and 23 gender- and age-matched controls. Urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2 were measured by previously validated radioimmunoassays. In addition, urinary immunoreactive leukotriene (LT) E4 was measured to explore the 5-lipoxygenase pathway of arachidonate metabolism. Polycythemic patients had significantly (P < .001) higher excretion rates of both 11-dehydro-TXB2 (1,033 +/- 1,050 v 117 +/- 45 pmol/mmol creatinine; mean +/- SD) and 2,3-dinor-TXB2 (725 +/- 676 v 82 +/- 43 pmol/mmol creatinine) than controls. In contrast, urinary LTE4 was not significantly different. Enhanced metabolite excretion did not correlate with the platelet count or with the hematocrit value, and was not related to the current treatment or to a clinical history of thrombotic complications. Platelet TX receptor studies did not show any significant changes in the binding characteristics of two different ligands. A platelet-selective regimen of aspirin therapy (50 mg/d for 7 to 14 days) was associated with greater than 80% suppression in metabolite excretion in nine patients. These results are consistent with abnormal stimuli operating in polycythemia vera to induce a selective enhancement in the platelet biosynthesis of TXA2 without changes in receptor binding. This in vivo abnormality in platelet biochemistry can be largely suppressed by low doses of aspirin.

scholarly journals Retention of dopamine 2 receptor mRNA and absence of the protein in craniospinal and extracranial metastasis of a malignant prolactinoma: a case report

2002 ◽  
pp. 81-88 ◽  
Author(s):  
J Winkelmann ◽  
U Pagotto ◽  
M Theodoropoulou ◽  
K Tatsch ◽  
W Saeger ◽  
...  
Keyword(s):  
Single Case ◽  
Clinical History ◽  
Extracranial Metastasis ◽  
Invasion And Metastasis ◽  
History Of ◽  
Dopamine 2 Receptor ◽  
Immunohistochemical Techniques

OBJECTIVES: The case presented here describes the clinical evolution of a malignant prolactinoma with occurrence of intra- and extra-cranial metastases. In this case, the presence of dopamine 2 receptor (D2R) was studied at the mRNA and protein level, in order to understand the pathological background of the resistance to treatment with different dopamine agonists. DESIGN: Together with an extensive description of the clinical history of this case, a combination of in vitro and in vivo techniques was performed to provide the basis of the dopamine resistance developed in the course of the disease. METHOD: A comparison of the D2R was performed in specimens obtained at presentation of the disease compared with autoptic specimens derived from local invasion and metastasis using in situ hybridization and immunohistochemical techniques. RESULTS: Intact D2R mRNA was found in the primitive tumor and metastatic tissues, whereas protein for the same receptor was present only in the tissues derived from neurosurgical operations and not in the metastases obtained post-mortem. CONCLUSION: This is the first report of the absence of D2R protein despite the retention of the transcript in an advanced stage of a malignant prolactinoma. The findings of this single case suggest the hypothesis that postranscriptional mechanisms may contribute to the development of dopamine resistance in prolactinomas.

scholarly journals Karyotypically distinct subpopulations in acute leukemia with specific growth requirements

Blood ◽  
1982 ◽  
Vol 59 (3) ◽  
pp. 641-645 ◽  
Author(s):  
B Lowenberg ◽  
A Hagemeijer ◽  
K Swart
Keyword(s):  
Leukemic Cell ◽  
Clinical History ◽  
Malignant Cell ◽  
Biological Properties ◽  
Myeloid Differentiation ◽  
Tumor Stem Cells ◽  
Growth Requirements ◽  
Acute Monoblastic Leukemia ◽  
History Of

Bone marrow and blood cells of a patient with acute monoblastic leukemia with subclones marked with specific karyotypic abnormalities were investigated. In order to more precisely evaluate the proliferative abilities of these populations, leukemic cell enriched fractions were prepared and incubated in two colony assays. Colony forming cells of the disparate clones had growth advantages in different systems which shows that their proliferation depended on the presence of selective stimulatory factors in culture. In one assay, at diagnosis, colonies from the minor clone were demonstrated exclusively. It is suggested that the assays measured distinct cellular stages of myeloid differentiation and the findings indicate that prior to diagnosis the neoplasm had evolved into subsets with progressive dedifferentiation. Differences of growth in vitro correlated with the different roles of these clones in the clinical history of the disease. Approaches based on differential cloning of tumor stem cells as in this example, may be useful for discriminating biological properties of heterogeneous subpopulations within neoplasms, and may facilitate the cytogenetic recognition of minimal clones among composite malignant cell specimens.

scholarly journals Food allergy and atopic dermatitis

2020 ◽  
Vol 2 (1) ◽  
pp. 35-38
Author(s):  
Tina Banzon ◽  
Donald Y.M. Leung ◽  
Lynda C. Schneider
Keyword(s):  
Atopic Dermatitis ◽  
Food Allergy ◽  
Immunoglobulin E ◽  
Growth Failure ◽  
Skin Barrier ◽  
Clinical History ◽  
Skin Inflammation ◽  
Specific Ige ◽  
Nutritional Deficiencies ◽  
Detailed Clinical History

Atopic dermatitis (AD), characterized by intense pruritus, eczematous lesions, and a relapsing disease course, is a chronic inflammatory skin disease that affects both children and adults. AD often begins in infancy and is associated with atopic diseases in the personal or family history.1 Environmental factors may trigger AD by affecting the skin barrier and by triggering inflammation. The elicitation of T-helper type 2 cytokines further impairs the epidermal barrier and leads to the penetration of irritants and allergens into the epidermis and thereby perpetuating inflammation. The presence of AD and its severity has been shown to positively correlate with risk of developing food allergy (FA). Children with AD are estimated to be six times more likely to develop FA compared with their healthy peers. It has been reported that nearly 40% of children with moderate-to-severe AD have immunoglobulin E (IgE) mediated FA compared with only 6% in the general population. Although analysis of experimental data has linked skin inflammation in AD to FA, with food challenges reproducing symptoms and avoidance diets improving AD, elimination diets are not known to cure AD and may have unfavorable consequences, such as loss of tolerance, which leads to immediate-type allergy, including anaphylaxis, nutritional deficiencies, growth failure, and reduction of quality of life for the patient and family. Exacerbation of AD can be inaccurately attributed to foods. Individuals with AD are often sensitized to foods with positive testing results, however, able to tolerate the food. In light of widespread ordering and commercial availability of serum specific IgE for FA, testing for FA is recommended only if, from a detailed clinical history, immediate-type allergic symptoms occur with ingestion of food, or in infants with AD who do not improve with optimal skin care.

New possibilities of thetherapy of patients with atopic dermatitis with Janus kinaseinhibitors

2021 ◽  
Author(s):  
Н.В. Зильберберг ◽  
М.М. Кохан ◽  
Ю.В. Кениксфест
Keyword(s):  
Atopic Dermatitis ◽  
Immune System ◽  
Skin Barrier ◽  
Specific Ige ◽  
Janus Kinase ◽  
Th2 Cells ◽  
First Year ◽  
Th2 Response ◽  
History Of ◽  
First Year Of Life

Атопический дерматит – широко распространенный хронический дерматоз мультифакториальной природы с превалирующей долей генетического компонента и сложным патогенезом. В патогенезе атопического дерматита важную роль играет наследственная детерминированность, приводящая к нарушению состояния кожного барьера, дефектам иммунной системы (стимуляция Th2-клеток с последующей гиперпродукцией IgE); гиперчувствительность к аллергенам и неспецифическим раздражителям, колонизации кожи и слизистых патогенными микроорганизмами, а также дисбаланс вегетативной нервной системы с повышением продукции медиаторов воспаления. К генетическим факторам развития атопического дерматита относят наличие мутации гена филаггрина, приводящей к нарушению функции эпидермального барьера при атопическом дерматите, а также семейный анамнез атопического дерматита и других атопических заболеваний. С дефектами иммунной системы связано развитие воспалительной реакции в коже с участием Т-лимфоцитов. В острую фазу заболевания преобладает Th2-ответ, когда происходит стимуляция Th2-клеток с последующей гиперпродукцией специфических IgE; в хроническую – происходит переключение с Th2- на Th1-иммунный ответ. В патофизиологические механизмы атопического дерматита вовлечены ряд интерлейкинов и ИФН-γ, которым для передачи сигнала требуется участие внутриклеточной сигнальной системы JAK/STAT, в том числе Янус-киназы 1-го типа. Заболевание развивается обычно в первые 2 года жизни и в 2/3 случаев сохраняется во взрослом возрасте, при этом 45% всех случаев начала заболевания приходится на первые 6 месяцев жизни: в 60% случаев заболевание развивается в течение первого года жизни и в 85% случаев в возрасте до 5 лет. В зрелом возрасте кожный процесс сохраняется у 38-42% больных. С течением времени подходы к терапии дерматоза претерпевали значительные изменения. В настоящей статье приведен актуальный обзор результатов клинических исследований препарата упадацитиниб в лечении больных атопическим дерматитом взрослых и подростков. Atopic dermatitis is a common chronic dermatosis of multifactorial nature with prevalence of genetic component and complex pathogenesis. In the pathogenesis of atopic dermatitis, an important role is played by hereditary determinism, leading to a violation of the state of the skin barrier, defects of the immune system (stimulation of Th2 cells with subsequent overproduction of IgE); hypersensitivity to allergens and nonspecific irritants, colonization of the skin and mucous membranes by pathogenic microorganisms, as well as an imbalance of the autonomic nervous system with an increase in the production of inflammatory mediators. The genetic factors for the development of atopic dermatitis include the presence of a mutation in the filaggrin gene, leading to dysfunction of the epidermal barrier in atopic dermatitis, as well as a family history of atopic dermatitis and other atopic diseases. The development of an inflammatory reaction in the skin with the participation of T-lymphocytes is associated with defects in the immune system. In the acute phase of the disease, the Th2 response predominates, when Th2 cells are stimulated with subsequent overproduction of specific IgE; in chronic – there is a switch from Th2- to Th1-immune response. A number of interleukins and IFN-γ, which require the participation of the JAK/STAT signaling system, including Janus kinase, are involved in the pathophysiological mechanisms of atopic dermatitis. The disease usually develops in the first 2 years of life, and in 2/3 of cases persists into adulthood, while 45% of all cases of onset of the disease occur in the first 6 months of life: in 60% of cases, the disease develops during the first year of life and in 85% cases under the age of 5 years. In adulthood, the skin process persists in 38-42% of patients. Over time, approaches to the treatment of thedermatosis have undergone significant changes. This article provides an up-to-date review of the results of clinical trials of the drug upadacitinib in the treatment of atopic dermatitis.

Karyotypically distinct subpopulations in acute leukemia with specific growth requirements

Blood ◽  
1982 ◽  
Vol 59 (3) ◽  
pp. 641-645 ◽  
Author(s):  
B Lowenberg ◽  
A Hagemeijer ◽  
K Swart
Keyword(s):  
Leukemic Cell ◽  
Clinical History ◽  
Malignant Cell ◽  
Biological Properties ◽  
Myeloid Differentiation ◽  
Tumor Stem Cells ◽  
Growth Requirements ◽  
Acute Monoblastic Leukemia ◽  
History Of

Abstract Bone marrow and blood cells of a patient with acute monoblastic leukemia with subclones marked with specific karyotypic abnormalities were investigated. In order to more precisely evaluate the proliferative abilities of these populations, leukemic cell enriched fractions were prepared and incubated in two colony assays. Colony forming cells of the disparate clones had growth advantages in different systems which shows that their proliferation depended on the presence of selective stimulatory factors in culture. In one assay, at diagnosis, colonies from the minor clone were demonstrated exclusively. It is suggested that the assays measured distinct cellular stages of myeloid differentiation and the findings indicate that prior to diagnosis the neoplasm had evolved into subsets with progressive dedifferentiation. Differences of growth in vitro correlated with the different roles of these clones in the clinical history of the disease. Approaches based on differential cloning of tumor stem cells as in this example, may be useful for discriminating biological properties of heterogeneous subpopulations within neoplasms, and may facilitate the cytogenetic recognition of minimal clones among composite malignant cell specimens.

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