Θεραπευτική προσέγγιση της Χρόνιας Ιδιοπαθούς Κνίδωσης

Η χρόνια κνίδωση αποτελεί ένα από τα πιο παράδοξα νοσήματα της ιατρικής.

Πρώτον, συμπεριφέρεται σαν ένα κλασσικό αλλεργικό νόσημα με σημεία και συμπτώματα τα οποία «μεσολαβούνται» από την ισταμίνη. Δεύτερον , χαρακτηρίζεται από την απουσία ευαισθητοποίησης, αλλά κυρίως κλινικής έκθεσης στην τριανδρία των κλασσικών ομάδων αλλεργιογόνων, δηλαδή τροφής, φαρμάκων και νυγμών από υμενόπτερα. Τρίτον, ένα σημαντικό ποσοστό της συσχετίζεται με αυτοαντισώματα. Με αδρούς λαϊκούς όρους, θα μπορούσε κανείς να ισχυρισθεί πως σταδιακά μεταβαίνουμε από το «αλλεργικό εξάνθημα» στο «αυτοάνοσο» εξανθημα. (1) Τέταρτον, η συμπτωματική ανταπόκριση της νόσου έναντι της «κορωνίδας» της αλλεργιολογίας, δηλαδή των anti-IgE αντισωμάτων (δραστική ουσία : omalizumab), είναι εντυπωσιακή.

Από τον παρακάτω διαδικτυακό σύνδεσμο μπορείτε να συμβουλευθείτε την προδημοσίευση ενός πρόσφατου άρθρου ανασκόπησης, του διεθνώς αναγνωρισμένου για το πολυετές έργο του στο αντικείμενο της χρόνιας κνίδωσης Allen Kaplan (2) , με θέμα την θεραπευτική προσέγγιση της χρόνιας κνίδωσης :

Allen P. Kaplan

Department of Medicine, Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, Medical University of South Carolina, Charleston, SC, USA.

Treatment of Chronic Spontaneous Urticaria.

Review.

Allergy Asthma Immunol Res. 2012 May;4:e114.

Published online 2012 May 14.

Copyright © 2012 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease.

pISSN 2092-7355 • eISSN 2092-7363

Η πρόσβαση στο πλήρες κείμενο του άρθρου είναι ελεύθερη :

http://e-aair.org/DOIx.php?id=10.4168/aair.2012.4.4.e114

ΠΕΡΙΛΗΨΗ.

Chronic spontaneous urticaria is defined as persistent symptoms of urticaria for 6 weeks or more. It is associated with autoimmunity in approximately 45 percent of patients. Therapy is often difficult however the initial approach should employ high-dose non-sedating antihistamines; 4-6 tablets/day may be necessary. It has been shown that the response to 4 tablets/day exceeds 3, and exceeds 2, which exceeds 1. However the dose that corresponds to the maximal dose of first generation antihistamines (hydroxyzine, diphenhydramine) used previously, is 6/day. Yet over half the patients are refractory to antihistamines and other agents should be tried next. Whereas current guidelines (published) often add leukotriene antagonists and/or H2 receptor antogonists next, these are of little utility. Likewise drugs effective for urticarial vasculitis (colchicine, dapsone, sulfasalazine, hydroxychloroquine) are effective in a small percentage of patients and no study suggests that the response rate of any of them exceeds the 30% placebo responses seen in most double-blind, placebo controlled studies. The drugs that are effective for antihistamine-resistant chronic spontaneous urticaria are corticosteroids, cyclosporine, and Omalizumab. Use of steroids is limited by toxicity. If used at all, a dose of no more than 10 mg/day should be employed with a weekly reduction of 1 mg. The response rates to cyclosporine and Omalizumab are each close to 75%. Cyclosporine can be used effectively if care is taken to monitor blood pressure, urine protein, blood urea nitrogen, and creatinine, every 6 weeks. Omalizumab has the best profile in terms of efficacy/toxicity and, once approved by federal agencies for use in chronic spontaneous urticaria, a dramatic change in the treatment paradigm, whether associated with autoimmunity or not, is predicted. A phase 3 trial is currently in place. Refractoriness to both Omalizumab and cyclosporine is expected to be less than 5 percent of patients. Other agents, can then be tried.

ΒΙΒΛΙΟΓΡΑΦΙΑ :

(1) : Di Lorenzo G, Leto-Barone MS, La Piana S, Seidita A, Rini GB.

Chronic spontaneous urticaria: an autoimmune disease? A revision of the literature.

Clin Exp Med. 2012 May 15. [Epub ahead of print] PubMed PMID: 22584681.

The cause of chronic spontaneous urticaria has been an enigma for decades, but the recognition of functional autoantibodies in some patients with the spontaneous chronic urticaria has opened up a new concept of autoimmune urticaria. Clinical and laboratory features are in keeping with an autoimmune aetiology for many patients with otherwise inexplicable disease, but there is still debate about the importance of functional autoantibodies in the disease pathogenesis, how to test them and the clinical implications for treatment and prognosis. This review will look at the evidence for there being an autoimmune subset of urticaria, the strengths and weaknesses of the available tests in current use.

(2) : Kaplan AP.

What the first 10,000 patients with chronic urticaria have taught me: a personal journey.

J Allergy Clin Immunol. 2009 Mar;123(3):713-7.

I became board certified in allergy and clinical immunology in 1974, and that was a period in which chronic urticaria was seriously considered by many to be an emotional disorder.

Currently, the major ideas concerning the cause, pathogenesis, or both of chronic urticaria are based on observations suggesting that it has an autoimmune cause in 40% to 45% of patients. There is the association with antithyroid antibodies, which appear to be a marker of autoimmunity; the pathogenic antibodies are IgG anti-IgE receptor or IgG anti-IgE.

I think chronic urticaria is pretty easy to treat, even if severe.