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1.
Aliment Pharmacol Ther ; 45(2): 300-309, 2017 01.
Article in English | MEDLINE | ID: mdl-27868216

ABSTRACT

BACKGROUND: Conflicting results have been recently reported for the accuracy of the Endoscopic Reference Score (EREFS), an standardised endoscopic classification, to predict the histological activity of eosinophilic oesophagitis (EoE). AIM: To evaluate the accuracy of the EREFS to predict either histological or clinical activity of EoE. METHODS: Prospective multicentre study conducted in eight Spanish centres evaluating adult EoE patients, either naïve or after treatment. Symptoms were evaluated before upper endoscopy through the Dysphagia Symptom Score, whereas researchers scored the EREFS immediately after the endoscopic procedure, unaware of the histological outcome. RESULTS: One hundred and forty-five EoE patients undergoing 240 consecutive endoscopic procedures were included. Exudates (P = 0.03), furrows (P = 0.03) and a composite score of inflammatory signs (exudates, furrows and oedema) (P < 0.001) accurately predicted histological activity. Exudates were the only endoscopic sign showing a good correlation with histological outcome after therapy. Furrows and oedema persisted in 50% and 70% of patients despite histological remission. No endoscopic feature exceeded 70% accuracy to predict histological activity. Likewise, no endoscopic finding could adequately predict dysphagia severity. Crepe paper mucosa, diffuse exudates and severe rings correlated with higher symptom scores. CONCLUSIONS: Endoscopic findings assessed by the Endoscopic Reference Score did not correlate with histological or clinical disease activity in adult EoE patients. Only exudates correlated with peak eosinophil count and histological outcome, whereas furrows and oedema persisted in over half of patients despite histological remission.


Subject(s)
Eosinophilic Esophagitis/pathology , Gastroscopy , Adult , Deglutition Disorders/diagnosis , Deglutition Disorders/immunology , Deglutition Disorders/pathology , Eosinophilic Esophagitis/diagnosis , Eosinophilic Esophagitis/immunology , Eosinophils/immunology , Esophagus/immunology , Esophagus/pathology , Female , Humans , Leukocyte Count , Male , Middle Aged , Mucous Membrane/immunology , Mucous Membrane/pathology , Prospective Studies , Reference Values , Young Adult
4.
Med. cután. ibero-lat.-am ; 37(5): 230-232, sept.-oct. 2009. ilus
Article in Spanish | IBECS | ID: ibc-80184

ABSTRACT

El imatinib es una inhibidor del enzima tirosin-quinasa. Se emplea en el tratamiento de la leucemia mieloide crónica, del dermatofibrosarcoma protuberansy de tumores gastrointestinales. Las reacciones cutáneas relacionadas con imatinib son frecuentes y suceden en un 9’5%-69% de los pacientes,según las series. Las más frecuentes son exantemas maculopapulosos, edemas generalizados y edema periorbitario. Hasta el momento se han descritopocos pacientes con erupciones liquenoides por imatinib. Presentamos un nuevo caso de erupción liquenoide por imatinib (AU)


Imatinib mesylate is a tyrosine kinase inhibitor. It is used to treat chronic myeloid leukaemia, dermatofibrosarcoma protuberans and gastrointestinalstromal tumours. Cutaneous reactions to imatinib are frequent and occur in 9’5-69% of patients, depending on the series reported. Maculopapulareruptions, generalized edema and periorbital edema are the most common adverse events observed. Lichenoid eruptions are very rare. We report anew case of imatinib-induced oral lichenoid eruption (AU)


Subject(s)
Humans , Male , Aged , Mouth Mucosa/pathology , Lichen Planus, Oral/chemically induced , Tyrosine/antagonists & inhibitors , Antineoplastic Agents/adverse effects , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy
5.
Adv Exp Med Biol ; 648: 105-12, 2009.
Article in English | MEDLINE | ID: mdl-19536471

ABSTRACT

Mechanisms involved in carotid body (CB) chemoreceptor cells O(2)-sensing and responses are not fully understood. So far, it is known that hypoxia depolarizes chemoreceptor cells via O(2)-sensitive K(+)-channel inhibition; calcium influx via voltage-gated channels and neurotransmitter secretion follow. Presence of high voltage activated (HVA) calcium channels in rat CB chemoreceptor cells is well documented, but the presence of low voltage activated (LVH) or T-type calcium channels has not been reported to date. The fact that O(2)-sensitive PC12 cells express T-type channels and that they are inducible by chronic hypoxia (CH) lead us to hypothesize they could be present and play a role in the genesis of the hypoxic response in rat CB chemoreceptor cells. We have analyzed the expression of the three isoforms of T-type calcium channels (alpha1G, alpha1H and alpha1I) and the isoforms alpha1C and alpha1D of L-type calcium channels in rat CB by RT-PCR. We found that rat CB expresses alpha1G and alpha1C subunits. After chronic hypoxic treatment of adult rats (10 degrees O(2), 8 days), expression of alpha1G seems to be down-regulated whereas alpha1C expression is up-regulated. Functionally, it was found that the release of catecholamine induced by hypoxia and high external K({+}) from CB chemoreceptor cells was fully sensitive to L-type channel inhibition (nisoldipine, 2 microM), while specific inhibition of T-channels (mibefradil, 2 microM) inhibited exclusively hypoxia-induced release (50 degrees ). As a whole, present findings demonstrate the presence of T-type as well as L-type calcium channels in rat CB and suggest a selective participation of the T-type channels in the hypoxic activation of chemoreceptor cells.


Subject(s)
Calcium Channel Blockers/pharmacology , Calcium Channels, L-Type/genetics , Calcium Channels, L-Type/metabolism , Calcium Channels, T-Type/genetics , Calcium Channels, T-Type/metabolism , Carotid Body/drug effects , Carotid Body/metabolism , Animals , Catecholamines/metabolism , DNA, Complementary/genetics , Gene Expression Regulation , Hypoxia/metabolism , In Vitro Techniques , Potassium/pharmacology , Protein Isoforms/genetics , Protein Isoforms/metabolism , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction
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