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1.
Journal of Korean Medical Science ; : e251-2022.
Artículo en Inglés | WPRIM | ID: wpr-938023

RESUMEN

Anaphylaxis to polyethylene glycol (PEG) is rare and mainly occurs with the use of laxatives containing PEG. Recently, an increasing number of PEG allergies have been reported, particularly those related to coronavirus disease 2019 (COVID-19) vaccines. mRNA COVID-19 vaccines, such as the BNT162b2 (Pfizer–BioNTech) and mRNA-1273 (Moderna) vaccines, contain PEG2000 as an excipient and are contraindicated when allergy to a vaccine component exist. We report a 55-year-old woman’s history as a case of successful mRNA COVID-19 vaccination and colonoscopy after oral desensitization to PEG in a patient with PEG allergy who required both COVID-19 vaccination and colon evaluation. Allergy to PEG was diagnosed based on clinical history, skin test results, and basophil histamine release testing. Oral desensitization effectively suppressed histamine release from basophils in response to PEG stimulation, suggesting that oral desensitization using PEG-based laxatives may be an effective treatment option for patients with allergy to the substance.

2.
The Korean Journal of Gastroenterology ; : 64-70, 2021.
Artículo en Inglés | WPRIM | ID: wpr-875409

RESUMEN

Esophageal motility disorders were re-defined when high-resolution manometry was employed to better understand their pathogenesis. Newly developed parameters including integrated relaxation pressure (IRP), distal contractile integral, and distal latency showed better diagnostic yield compared with previously used conventional parameters. Therefore, Chicago classification was formulated, and its diagnostic cascade begins by assessing the IRP value. However, IRP showed limitation due to its inconsistency, and other studies have tried to overcome this. Recent studies showed that provocative tests, supplementing the conventional esophageal manometry protocol, have improved the diagnostic yield of the esophageal motility disorders. Therefore, position change from supine to upright, solid or semi-solid swallowing, multiple rapid swallows, and the rapid drink challenge were newly added to the manometry protocol in the revised Chicago classification version 4.0. Impedance planimetry enables measurement of bag cross-sectional area at various locations. The functional lumen imaging probe (FLIP) has been applied to assess luminal distensibility. This probe can also measure pressure, serial cross-sectional areas, and tension-strain relationship. The esophagogastric junction’s distensibility is decreased in achalasia. Therefore, EndoFLIP can be used to assess contractility and distensibility of the esophagus in the patients with achalasia, including repetitive antegrade or retrograde contractions. EndoFLIP can detect achalasia patients with relatively low IRP, which was difficult to diagnose using the current high-resolution manometry. EndoFLIP also provides information on the contractile activity and distensibility of the esophageal body in patients with achalasia. The use of provocative tests, newly added in Chicago classification 4.0 version, and EndoFLIP can expand understanding of esophageal motility disorders.

3.
Electrolytes & Blood Pressure ; : 12-16, 2017.
Artículo en Inglés | WPRIM | ID: wpr-29649

RESUMEN

Posterior reversible encephalopathy syndrome (PRES) is characterized by a clinical and radiological entity with the sudden onset of seizures, headache, altered consciousness, and visual disturbances in patients with the findings of reversible vasogenic subcortical edema without infarction. Hypertension, renal disease, and autoimmune disease are co-morbid conditions of PRES. Nevertheless, there have only been a few case reports of PRES in a patient with anti-glomerular basement membrane antibody glomerulonephritis (anti-GBM GN). This paper presents the possible first Korean case of a 36-year-old woman with the striking features of PRES. She presented with a sudden onset of visual blindness, headache, and seizure. The brain MRI images revealed hyperintense lesions in both the occipital and parietal lobes, which suggested vasogenic edema. Three months before this presentation, she was diagnosed with anti-GBM GN. Since then, she underwent immunosuppression with cyclophosphamide and steroid, and hemodialysis for renal failure with a treatment of anti-GBM GN.


Asunto(s)
Adulto , Femenino , Humanos , Enfermedades Autoinmunes , Membrana Basal , Ceguera , Encéfalo , Estado de Conciencia , Ciclofosfamida , Edema , Glomerulonefritis , Cefalea , Hipertensión , Hipertensión Renal , Terapia de Inmunosupresión , Infarto , Imagen por Resonancia Magnética , Lóbulo Parietal , Síndrome de Leucoencefalopatía Posterior , Diálisis Renal , Insuficiencia Renal , Convulsiones , Huelga de Empleados
4.
Yonsei Medical Journal ; : 862-866, 2015.
Artículo en Inglés | WPRIM | ID: wpr-137565

RESUMEN

Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-kappaB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present study is to determine whether H. pylori-induced activation of NF-kappaB and the expression of interleukin-8 (IL-8) are mediated by the activation of Jak1/Stat3 in gastric epithelial (AGS) cells. Thus, gastric epithelial AGS cells were infected with H. pylori in Korean isolates (HP99) at bacterium/cell ratio of 300:1, and the level of IL-8 in the medium was determined by enzyme-linked immonosorbent assay. Phospho-specific and total forms of Jak1/Stat3 and IkappaBalpha were assessed by Western blot analysis, and NF-kappaB activation was determined by electrophoretic mobility shift assay. The results showed that H. pylori induced the activation of Jak1/Stat3 and IL-8 production, which was inhibited by a Jak/Stat3 specific inhibitor AG490 in AGS cells in a dose-dependent manner. H. pylori-induced activation of NF-kappaB, determined by phosphorylation of IkappaBalpha and NF-kappaB-DNA binding activity, were inhibited by AG490. In conclusion, Jak1/Stat3 activation may mediate the activation of NF-kappaB and the expression of IL-8 in H. pylori-infected AGS cells. Inhibition of Jak1/Stat3 may be beneficial for the treatment of H. pylori-induced gastric inflammation, since the activation of NF-kappaB is inhibited and inflammatory cytokine expression is suppressed.


Asunto(s)
Humanos , Western Blotting , ADN Bacteriano/análisis , Células Epiteliales/metabolismo , Mucosa Gástrica/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Regulación Bacteriana de la Expresión Génica , Infecciones por Helicobacter/inmunología , Helicobacter pylori/genética , Interleucina-8/genética , Janus Quinasa 1 , FN-kappa B/biosíntesis , Fosforilación , ARN Mensajero/metabolismo , Factor de Transcripción STAT3 , Transducción de Señal/genética
5.
Yonsei Medical Journal ; : 862-866, 2015.
Artículo en Inglés | WPRIM | ID: wpr-137564

RESUMEN

Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-kappaB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present study is to determine whether H. pylori-induced activation of NF-kappaB and the expression of interleukin-8 (IL-8) are mediated by the activation of Jak1/Stat3 in gastric epithelial (AGS) cells. Thus, gastric epithelial AGS cells were infected with H. pylori in Korean isolates (HP99) at bacterium/cell ratio of 300:1, and the level of IL-8 in the medium was determined by enzyme-linked immonosorbent assay. Phospho-specific and total forms of Jak1/Stat3 and IkappaBalpha were assessed by Western blot analysis, and NF-kappaB activation was determined by electrophoretic mobility shift assay. The results showed that H. pylori induced the activation of Jak1/Stat3 and IL-8 production, which was inhibited by a Jak/Stat3 specific inhibitor AG490 in AGS cells in a dose-dependent manner. H. pylori-induced activation of NF-kappaB, determined by phosphorylation of IkappaBalpha and NF-kappaB-DNA binding activity, were inhibited by AG490. In conclusion, Jak1/Stat3 activation may mediate the activation of NF-kappaB and the expression of IL-8 in H. pylori-infected AGS cells. Inhibition of Jak1/Stat3 may be beneficial for the treatment of H. pylori-induced gastric inflammation, since the activation of NF-kappaB is inhibited and inflammatory cytokine expression is suppressed.


Asunto(s)
Humanos , Western Blotting , ADN Bacteriano/análisis , Células Epiteliales/metabolismo , Mucosa Gástrica/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Regulación Bacteriana de la Expresión Génica , Infecciones por Helicobacter/inmunología , Helicobacter pylori/genética , Interleucina-8/genética , Janus Quinasa 1 , FN-kappa B/biosíntesis , Fosforilación , ARN Mensajero/metabolismo , Factor de Transcripción STAT3 , Transducción de Señal/genética
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